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Prepublished online as a Blood First Edition Paper on June 26, 2003; DOI 10.1182/blood-2002-10-3207. This Article Full Text (PDF) All Versions of this Article: 2002-10-3207v1 102/7/2632    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Canitrot, Y. Articles by Skorski, T. Search for Related Content PubMed PubMed Citation Articles by Canitrot, Y. Articles by Skorski, T. Social Bookmarking                   What's this? Submitted October 22, 2002 Accepted June 9, 2003 p210 BCR/ABL kinase regulates nucleotide excision repair (NER) and resistance to ultraviolet (UV) radiation Yvan Canitrot, Rafal Falinski, Thierry Louat, Guy Laurent, Christophe Cazaux, Jean-Sebastien Hoffmann, Dominique Lautier, and Tomasz Skorski* Genetics Instability and Cancer, Institut de Pharmacologie et Biologie Structurale, Toulouse, France Center for Biotechnology, Temple University, Philadelphia, PA, USA Institut Claudius Regaud, INSERM UR563, Toulouse, France CHU Purpan, Service Hematologie, Toulouse, France * Corresponding author; email: tskorski{at}astro.temple.edu. Both clinical and experimental evidence illustrate that p190 and p210 BCR/ABL oncogenic tyrosine kinases induce resistance to DNA damage and confer an intrinsic genetic instability. Here, we investigated whether BCR/ABL expression could modulate nucleotide excision repair (NER). We found that ectopic expression of p210 BCR/ABL in murine lymphoid BaF3 cell line inhibited NER activity in vitro, promoting hypersensitivity of these cells to UV treatment and facilitating a mutator phenotype. However, expression of p210 BCR/ABL in human and murine myeloid cell lines and primary bone marrow cells resulted in the increased NER activity and resistance to UV irradiation. The ABL tyrosine kinase inhibitor STI571 reversed these effects showing that p210 BCR/ABL tyrosine kinase activity is responsible for de-regulation of NER. Hypo-activity of NER in p210 BCR/ABL-positive lymphoid cells was accompanied by the decreased interaction between PCNA and XPB; conversely, this interaction was enhanced in p210 BCR/ABL-positive myeloid cells. p190 BCR/ABL did not affect NER in lymphoid and myeloid cells. In summary, our study suggests that p210 BCR/ABL reduced NER activity in lymphoid cells leading to hypersensitivity to UV and mutagenesis. 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